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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied pulmonary haemodynamics in 19 male patients, mean age 45 +/- 5 years, suffering from severe OSA, mean apnea/hypopnea index (AHI) 68 +/- 17. Pulmonary haemodynamisc were studied using Swan-Ganz thermodilution catheter in the supine position at rest, and at the end of the 7th minute of steady-state exercise (40 W). Investigations were repeated after one year of treatment with nasal CPAP. At rest mean pulmonary artery pressure (PPA), pulmonary wedge pressure (PW) and cardiac output (CO) were normal, PPA = 16.6 +/- 5.7 mmHg, PW = 5.2 +/- 1.8 l/min. Pulmonary vascular resistance (PVR) was slightly elevated = 155 +/- 65 d.sec.cm-5. On exercise only PVR remained unchanged. After a year of treatment PPA changed to 15.8 +/- 4.0 mmHg (NS), Pw-7.5 +/- 3.1 mmHg (NS), CO-4.9 +/- 1.6 L/min (NS), PVR - 145 +/- 35 d.sec.cm-5 (NS). In two patients with resting hypertension PPA dropped from 33 mmHg to 25 mmHg and 28 mmHg to 18 mmHg respectively. Statistical analysis showed no significant change in any of the studied variables after one year of the CPAP therapy.
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PMID:[Pulmonary circulation at rest and during exercise in patients with obstructive sleep apnea before and after one year of treatment with CPAP]. 899 59

The aim of this randomized controlled trial was to assess the effects of treatment with continuous positive airway pressure versus conservative therapy (CT) on well-being, mood, and functional status in subjects with mild sleep-disordered breathing (SDB). One hundred and eleven subjects, aged 25 to 65 yr, with a respiratory disturbance index (RDI) of 5 to 30 and without subjective pathologic sleepiness, were randomized to nasal CPAP or to CT. Ninety-seven subjects were followed-up after 8 wk. Treatment response was assessed from changes between baseline and follow-up measures of mood, energy/fatigue, and functional status/general health. Of the 51 subjects randomized to CPAP, 25 (49%) experienced an improved outcome, as compared with 12 of 46 of subjects (26%) randomized to CT (p < 0.05). The odds of experiencing a treatment response in the CPAP as compared with the CT group were 2.72 (OR: 1.18 to 6.58, 95% CI). A beneficial effect of CPAP over CT was most evident among individuals without sinus problems and among subjects with hypertension or diabetes. Differential treatment responses were not related to degree of baseline sleepiness or SDB. This suggests that middle-aged snorers with relatively low levels of SDB (RDI < 30) may benefit more from nasal CPAP than from less specific therapy directed at improving breathing during sleep. CPAP therapy may be beneficial to a broader group of subjects than previously appreciated.
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PMID:Improvement of mild sleep-disordered breathing with CPAP compared with conservative therapy. 951 3

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of new techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long term cardiovascular morbidity is not established.
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PMID:[Autonomic nervous system and obstructive sleep apneas]. 1047 34

There is clear evidence for obstructive sleep apnea as an independent cause of arterial hypertension. We report a case of intracranial hemorrhage with systemic hypertension resistant to antihypertensive medication, which could only be adjusted after effective treatment of coexisting sleep-disordered breathing. The 36 year old male (body mass index 31 kg/m2) was admitted to hospital three weeks before for intracranial bleeding at the left external capsule. Diagnosis of primary hypertension was made after extensive work-up in the acute hospital. Blood pressure was adjusted with five-fold antihypertensive medication at the time of admission to neurological rehabilitation, but was still elevated with "non-dipping" as determined by long-term measurement despite medications above the recommended dosages. Polysomnography confirmed the diagnosis of obstructive sleep apnea. 10 days after initiation of treatment with nasal CPAP blood pressure control was easier with normal dipping at night. Medication could be reduced during rehabilitation with further reduction after discharge. Moderate obstructive sleep apnea appears to be the cause of severe hypertension resistant to pharmacological therapy in this patient. The case underlines the impact of diagnosis and treatment of sleep-disordered breathing for the secondary prevention of stroke.
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PMID:[Obstructive sleep apnea syndrome. A probably cause of therapy refractory hypertension in intracerebral hemorrhage]. 1055 87

This paper reviews some of the recent advances in the sleep apnoea/hypopnoea syndrome. Sleep apnoea has recently been shown to be familial and in some of these patients this is due to retroposition of the maxilla and mandible. There is now good evidence that individuals with sleep apnoea have an increased risk of road accidents and increasing, although not yet 100% robust, evidence that they have an increased frequency of systemic hypertension. The last few years have seen a large number of randomised controlled trials of CPAP therapy which have shown clear evidence that CPAP improves symptoms, subjective sleepiness, objective sleepiness, cognitive function, IQ, mood, quality of life and driving ability. Evidence that CPAP influences cardiovascular and cerebrovascular outcomes is awaited.
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PMID:Sleep and breathing. 1072 85

The cardiovascular sequelae best shown to be associated with OSA are systemic hypertension and acute vascular events. The cardiovascular sequelae, including acute myocardial infarction or nocturnal angina may be contributed to by arterial vasospasm or clot formation in the area of an atheroma. Thus far there are no data showing that treatment of OSA eliminates vascular sequelae, but much evidence shows that chronic CPAP therapy may lower elevated blood pressure in some patients. However, for a variety of reasons mentioned above, CPAP does not correct hypertension in all OSA patients.
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PMID:Cardiovascular effects of continuous positive airway pressure in obstructive sleep apnea. 1089 92

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of new techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory maneuvers. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long term cardiovascular morbidity is not established.
 ...
PMID:[Autonomic nervous system and sleep apnea syndromes]. 1093 4

Obstructive Sleep Apnea(OSA) is associated with an increased prevalence of cardiovascular complication such as systemic hypertension, ischemic heart disease and stroke, which may lead to unexpected or early death. Sleep in patients with OSA demonstrates a pattern of recurrent arousals, hemodynamic changes, and sympathetic neural activity that have been associated with adverse carviovascular events following awakening in the morning. Neurologic problems in patients with OSA include cognitive impairment, poor memory, and high risk for cerebral infarction. These central nervous system symptoms might be due to hypoxemia and sleep fragmentations. The vascular endothelial damage, platelet aggregation, and hemodynamic changes during sleep apnea are influenced by changes in oxygen and carbon dioxide tension inducing alterations of vascular tone. The cerebral hemodynamics in relation to apneas may not only influence daytime cerebral symptoms but may also have implications for the generation of cerebrovascular disease in OSA. These changes resulted from OSA might play an important role in pathophysiological aspects of the central nervous system. And these changes will be improved after CPAP application.
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PMID:[Abnormality of blood congulation]. 1094 24

In the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of repetitive episodes of hypoxia, hypercapnea, arousals, and a striking surge in sympathetic excitation, and altered baroreflex control during sleep. Obstructive sleep apnea (OSA) may lead to the cardiac arrhythmias and myocardial ischemia and it is a possible risk factor for stroke. We confirmed that nasal CPAP has been shown to lower blood pressure in some hypertensive OSA patients. Early recognition and treatment of sleep-apnea may improve cardiovascular function.
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PMID:[Hypertension and altered cardiovascular variability associated with obstructive sleep apnea]. 1094 41

Nasal continuous positive airway pressure (n-CPAP) is an effective treatment for the obstructive sleep apnea syndrome (OSAS). It is currently regarded as the first line therapy for OSAS. The principal indication for n-CPAP treatment is daytime sleepiness. Nasal-CPAP improves daytime sleepiness dramatically in severe cases and the effect is objectively measurable with the multiple sleep latency test (MSLT). It is noteworthy that n-CPAP also improves symptoms, subjective daytime sleepiness, cognitive function, IQ, mood, quality of life and driving ability already in patients with mild sleep apnea with an apnea/hypopneaindex (AHI) between 5 and 15 per hour of sleep during overnight polysomnography. Although not yet 100% robust, there is clear evidence that patients with OSAS have an increased frequency of systemic hypertension. Some early and imperfect studies suggest that CPAP reduces cardiovascular and cerebrovascular outcomes; however unequivocal evidence that n-CPAP reduces mortality is still awaited. There is now good evidence that treatment with n-CPAP reduces the two- to sevenfold increased risk of road accidents of untreated patients with OSAS. In summary, there exists abundant evidence today that n-CPAP is an efficient therapy for symptomatic patients with the obstructive sleep apnea syndrome. A trial with n-CPAP is therefore justified in all symptomatic patients. Based on the large number of randomized controlled trials of n-CPAP a therapeutic trial is indicated even in only mildly symptomatic patients with OSAS. Nasal-CPAP use and outcomes of therapy can be improved by provision of an intensive CPAP-education and support program.
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PMID:[Effectiveness of nasal CPAP-treatment (continuous positive airway pressure)]. 1095 51


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